Medical Inspection – Health Blog

In our diet, protein is the principal source of non-volatile, so- called fixed acids, which are eliminated via the kidneys, through the production of ammonium ions and titratable acidity. Their acidifying effect is linked to the metabolism of sulphate aminoacids (methionine and cysteine) which produce H+ and generate an increase in the renal excretion of calcium through the direct tubular mechanism and, when in excess, via a giving up of bone calcium. This is the metabolic basis that explains the well-documented hypercalciuria when the diet contains an excess of protein, particularly of animal origin. On the oth­er hand, it is known that, also in stone formers, the reduction in animal protein is able to significantly reduce the excretion of calcium. This knowledge is consistent with the epidemio- logical data showing that an intake of animal protein in excess of 76 g/day is able to increase by 33% the risk of forming kid­ney stones. The calciuretic effect of proteins is partly re­duced by the contemporary administration of alkaline salts such potassium bicarbonate or potassium citrate so, in dietary terms, in addition to a reduction in proteins, it could be impor­tant to increase the intake of alkaline potassium via an ade­quate consumption of fruit and vegetables. It is also necessary to consider that the proteins of vegetable origin (soya, chick­peas, French beans, broad beans, peas, lentils) have a lower sulphur aminoacids content and are therefore preferable for hy- percalciuric subjects. Canadian Drugstore canadian healthcare shop item

As already mentioned, the alkaline potassium found in fruit and vegetables is important for reducing the calciuretic effect of proteins, but not only for this reason. A depletion of potassium in itself is accompanied by an increase in calciuria and, on the other hand, its addition in the form of potassium citrate or potassium bicarbonate can reduce the calciuria significantly. The mechanism could be linked to the variations in intra­cellular pH in the acidic sense when there is potassium deple­tion, and in the alkaline sense when there is high potassium availability. Also in this case there is strong epidemiological ev­idence: in both men and women a high potassium intake (greater than 103 mEq/day) reduces the risk of stone formation by more than 50% in comparison with a low intake. Therefore, an important recommendation in idiopathic hypercalciuria is also that of consuming a reasonable quantity of fruit and vegetables on a regular basis, taking care to choose prod­ucts with a relatively low oxalate content to avoid increases in oxaluria. One cannot ignore the fact that some fruit juices have been shown to significantly increase the urinary citrate, which is a very good inhibitor of calcium oxalate crystallization. It is not possible to measure with accuracy the salt consump­tion of a person, but given that dietary sodium chloride is al­most completely absorbed in the intestine and eliminated in the urine, its consumption can be easily deduced by measuring its renal excretion. Kleeman et al. were the first to demonstrate that the increase of sodium chloride in the diet of normal sub­jects provoked an increase in the excretion of calcium. Various authors then confirmed the existence of a strict rela­tionship between the intake of sodium chloride and calciuria, in both normal and hypercalciuric subjects, and some experi­ences have been indicated where idiopathic hypercalciuria was corrected with the simple restriction of salt in the diet. Also on the epidemiological level, it could be detected that when the consumption of sodium exceeded certain levels, the risk of forming kidney stones increased. Many authors, when speaking of salt, make reference to sodium.

But, to be more exact, it should be said that it does not appear that the sodium ion is responsible for the increase in calciuria, but rather the chloride ion. A study to clarify the situation was performed by Muldowney et al. in 1994. These Authors indicated that when supplementing the diet with a certain quantity of sodium chloride there was a marked increase in calciuria, but when the same diet is supplemented with an equimolecular quantity of sodium bicarbonate, the increase in calciuria is not produced. Finally, it should also be kept in mind that the calciuretic effect of sodium chloride is summed with that of animal proteins and, vice versa, when sodium chloride is removed from the di­et, the calciuretic effect of the potassium depletion is prevented. So the consumption of table salt or the intake of exces­sive quantities of foods which, because of their nature or indus­trial processing, contain a lot of salt should be strongly limited in hypercalciuric subjects. In addition, those same mechanisms through which the sodium chloride increases the calciuria, in other words the expansion of the extracellular volume and the tubular competition of the two cations for their reabsorption, al­so seems to cause an increase in arterial pressure in salt-sen­sitive subjects.

Therefore, the limitation of salt could be decisive also for re­ducing the blood pressure of patients similar to the subject that we presented.

The above-mentioned epidemiological study has also identified the influence of sucrose on stone risk. Subdividing the pop­ulation under investigation in relation to the use of sucrose, it was seen that increasing quantities of sugar are accompanied by increasing risk levels, double the risk being reached with an intake greater than 56 g/day. An explanation of this fact would seem to lie in the well-known effect that sugars have on the se­cretion of insulin. Every time that there is a dietary load of sug­ars, especially simple sugars, there is a blood-insulin peak which is proportional to the load and, in some so-called insulin-resistant subjects, it is exaggerated with respect to the load. A high pro­portion of overweight and/or hypertensive people are seen to have this metabolic anomaly which is described as insulin-resis­tance. Holl and Allen, in 1987, published results showing a strict positive correlation between the levels of insulin in the serum, caused by a sugar load, and an increase in urinary calci­um. It is probable than insulin acts directly on the renal tubule re­ducing its capacity to reabsorb calcium. This fact explains the various studies that have indicated a constant and significant in­crease in calciuria in conditions of oral intake of simple sugars. This phenomenon, which is repeated intermittently dur­ing the day, could generate peaks of calcium oxalate supersatu- ration in the urine which are responsible for an increased litho- genic risk. Therefore, the limitation in the daily consumption of sugars, especially simple sugars, must also enter into the dietary norms which concern idiopathic hypercalciuria. The principal dietary norms that are useful for the prevention of idiopathic hypercalciuria are summarized in Table III. It is not easy to maintain with constancy, and over a long peri­od of time, a good adherence to the type of diet recommended, but the results convince both the doctor and the patient to make a concerted effort.